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Targeting Long Noncoding RNA HMMR-AS1 Suppresses and Radiosensitizes Glioblastoma

Junyang Li1, Xiangjun Ji1, Handong Wang1

  • 1Department of Neurosurgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, 210002, China.

Neoplasia (New York, N.Y.)
|March 26, 2018
PubMed

Insights

Long noncoding RNA HMMR-AS1 promotes glioblastoma (GBM) growth by stabilizing the oncogene HMMR. Targeting HMMR-AS1 inhibits GBM progression and enhances radiosensitivity by reducing DNA repair proteins.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long noncoding RNAs (lncRNAs) are implicated in cancer development.
  • The HMMR oncogene drives glioblastoma (GBM) progression.
  • The regulatory role of lncRNAs on HMMR in GBM is currently unknown.

Purpose of the Study:

  • To investigate the role of lncRNAs in regulating HMMR expression in glioblastoma.
  • To identify specific lncRNAs that interact with HMMR in GBM.
  • To explore the therapeutic potential of targeting these lncRNAs in GBM treatment.

Main Methods:

  • Identification and characterization of HMMR-AS1 in GBM cell lines.
  • Assessment of HMMR-AS1's effect on HMMR mRNA stability.
  • In vitro and in vivo experiments evaluating the impact of HMMR-AS1 knockdown on GBM cell behavior and tumor growth.
  • Analysis of DNA repair protein expression following HMMR-AS1 knockdown.

Main Results:

  • HMMR antisense lncRNA (HMMR-AS1) is overexpressed in GBM and stabilizes HMMR mRNA.
  • Knockdown of HMMR-AS1 decreases HMMR expression, inhibiting GBM cell migration, invasion, and mesenchymal phenotypes.
  • HMMR-AS1 knockdown suppresses GBM cell growth in vitro and in vivo.
  • Reducing HMMR-AS1 sensitizes GBM to radiation by downregulating DNA repair proteins ATM, RAD51, and BMI1.

Conclusions:

  • HMMR-AS1 acts as a crucial regulator of HMMR in GBM through sense-antisense interference.
  • Targeting HMMR-AS1 represents a promising therapeutic strategy for glioblastoma, potentially overcoming radioresistance.

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